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KIF3C Promotes the Malignant Progression of Lung Cancer Cells A549
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作者 haiwang liu Ran liu +2 位作者 Meiling Hao Xing Zhao Chunhui Li 《Proceedings of Anticancer Research》 2022年第6期1-7,共7页
Objective:To investigate the role of KIF3C gene in promoting the malignant phenotype of lung cancer cells and in regulating PI3K/AKT signaling pathway.Methods:CCK-8 and transwell assays were used to detect the changes... Objective:To investigate the role of KIF3C gene in promoting the malignant phenotype of lung cancer cells and in regulating PI3K/AKT signaling pathway.Methods:CCK-8 and transwell assays were used to detect the changes in cell proliferation and cell migration ability after being transfected with siKIF3C,as well as the protein expression levels of PI3K,p-PI3K,AKT,and p-AKT following the downregulation of KIF3C by Western blot.Results:The CCK-8 assay showed that the proliferation/viability of lung cancer cells A549 significantly reduced after being transfected with siKIF3C gene(P<0.05);the migration ability of lung cancer cells A549 was significantly reduced after transfected with siKIF3C gene(P<0.05);the levels of p-PI3K and p-AKT proteins were downregulated after KIF3C protein knockdown(P<0.05);however,the detection of PI3K and AKT protein levels was not statistically significant.Conclusion:KIF3C may promote the proliferation and migration ability of lung cancer cells A549 through PI3K/AKT signaling pathway. 展开更多
关键词 KIF3C A549 EMT Lung cancer
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Knockdown of KIF3C Inhibits Epithelial-Mesenchymal Transition in Lung Cancer Cells A549
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作者 haiwang liu Ran liu +2 位作者 Meiling Hao Xing Zhao Chunhui Li 《Journal of Clinical and Nursing Research》 2022年第5期50-56,共7页
The objective of this study is to reveal the role of KIF3C gene in the proliferation of lung cancer cells,and the regulation of epithelial mesenchymal transition(EMT)of tumor cells.The plate clone formation assay and ... The objective of this study is to reveal the role of KIF3C gene in the proliferation of lung cancer cells,and the regulation of epithelial mesenchymal transition(EMT)of tumor cells.The plate clone formation assay and cell scratch assay were used in this study to detect the changes of cell proliferation and migration ability after siKIF3C interference,while EMT-related protein expression after KIF3C downregulation was detected by Western blot.The cell clone formation assay showed that the number of clones of lung cancer cells A549 was significantly reduced after transfected with siKIF3C(P<0.05);The scratch assay showed that the healing ability of cells was significantly reduced after transfected with siKIF3C(P<0.05);Western blot protein analysis revealed that the levels of EMT-related proteins,N-cadherin,Vimentin,Snail,and Slug were significantly down-regulated(P<0.05),however,E-cadherin protein levels were up-regulated after siKIF3C interference.In conclusion,KIF3C may promote the proliferation and invasive ability of lung cancer cells A549 through EMT. 展开更多
关键词 KIF3C A549 EMT Lung cancer
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miR-186下调KIF3C抑制PI3K/AKT信号通路抗肺癌细胞的增殖、迁移和侵袭
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作者 刘海旺 刘燃 +2 位作者 郝美玲 赵醒 李春辉 《湖南师范大学学报(医学版)》 2022年第5期21-28,共8页
目的 :探究驱动蛋白家族成员3C(kinesin family member 3C,KIF3C)和微小RNA(mircoRNA,miR)-186对人肺癌细胞增殖、迁移和侵袭的影响及其调控机制。方法 :体外培养人肺癌A549细胞系,然后转染miR-186mimics、miR-186 inhibitor、siRNA(si)... 目的 :探究驱动蛋白家族成员3C(kinesin family member 3C,KIF3C)和微小RNA(mircoRNA,miR)-186对人肺癌细胞增殖、迁移和侵袭的影响及其调控机制。方法 :体外培养人肺癌A549细胞系,然后转染miR-186mimics、miR-186 inhibitor、siRNA(si)-KIF3C、miR-186 inhibitor+si-KIF3C及mimic NC、inhibitor NC和si-NC至A549细胞,分别设为miR-186 mimic组、miR-186 inhibitor组、si-KIF3C组、miR-186 inhibitor+si-KIF3C组及NC组(mimic NC组、inhibitor NC组和si-NC组),非转染的细胞设为Con组。用实时荧光定量PCR(real-time quantitative PCR,RT-qPCR)测定A549细胞中miR-186及KIF3C基因表达水平;蛋白免疫印迹(western blotting,WB)法测定KIF3C和磷脂酰肌醇-3激酶/丝氨酸苏氨酸蛋白激酶(phosphatidylinositol 3 kinase/serine threonine protein kinase,PI3K/AKT)通路相关蛋白表达水平;活细胞计数试剂盒-8(cell counting kit-8,CCK-8)测定细胞活力;5-乙炔基-2’脱氧尿嘧啶核苷(5-ethynyl-2’deoxyuracil nucleoside,EdU)法测定细胞增殖;Transwell小室测定细胞的迁移和侵袭。结果 :miR-186 mimic组miR-186表达水平显著高于mimic NC组(P<0.05),miR-186 inhibitor组miR-186表达水平显著低于inhibitor NC组(P<0.05),si-KIF3C组KIF3C mRNA和蛋白表达水平显著低于si-NC组(P<0.05),以上实验证明了miR-186 mimic、miR-186 inhibitor和si-KIF3C转染成功。与NC组相比,miR-186 mimic组和siKIF3C组细胞活力、增殖率、迁移数、侵袭数及KIF3C、p-PI3K和p-AKT蛋白表达水平显著降低,miR-186 inhibitor组则显著升高(P<0.05);miR-186 inhibitor+si-KIF3C组上述指标显著低于miR-186 inhibitor组,显著高于siKIF3C组(P<0.05)。结论 :过表达miR-186通过下调KIF3C抑制肺癌细胞的增殖、迁移和侵袭,其作用机制可能是抑制PI3K/AKT信号通路有关。 展开更多
关键词 肺癌 miR-186 驱动蛋白家族成员3C 磷脂酰肌醇-3激酶/丝氨酸苏氨酸蛋白激酶信号通路 增殖 迁移 侵袭
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Optically“silent”neptunium(Ⅴ)-nitrate complex in ionic liquid
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作者 Xue Dong Zhipeng Wang +5 位作者 Qiang Yan haiwang liu Yuxiao Guo Hong Cao Jing Chen Chao Xu 《Chinese Chemical Letters》 SCIE CAS CSCD 2022年第7期3531-3533,共3页
The complexation of pentavalent neptunium,Np(Ⅴ),with nitrate ion in an ionic liquid solution has been studied spectroscopically for the first time.The characteristic f-f transition absorption band of Np(Ⅴ)in the NIR... The complexation of pentavalent neptunium,Np(Ⅴ),with nitrate ion in an ionic liquid solution has been studied spectroscopically for the first time.The characteristic f-f transition absorption band of Np(Ⅴ)in the NIR region changes significantly upon the titration of nitrate ion into the solution,revealing strong complexation of Np(Ⅴ)with nitrate ion in the ionic liquid.Most notably,the absorption band of Np(Ⅴ)almost disappears when a sufficiently high concentration of nitrate ion is present in the solution.Such a rare optically“silent”species can be assigned to the 1:2 Np(Ⅴ)/nitrate complex with a centrosymmetric coordination environment where Np sits at the inversion center. 展开更多
关键词 NEPTUNIUM Ionic liquid COMPLEXATION ABSORPTION f-f transition
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